A cancer is a malignant tumor of potentially unlimited growth. It is primarily the pathogenic replication (a loss of normal regulatory control) of various given types of cells found in the human body. By select mutation resulting from a primary lesion, the DNA of a cancer cell evolves and converts the cell into an autonomous system. Conventional cancer treatments have focused mainly on killing cancerous cells. Such treatments threaten noncancerous cells, inherently are stressful to the human body, produce many side effects, and are of uncertain efficacy. More important, such treatment regimens are not ordinarily directed toward the actual chemical bond root of the cancer problem.
Cancer cells possess uncontrolled replication. Such uncontrolled replication readily can be caused by a chemical bond lesion in the cell's deoxyribonucleic acid (DNA). Specifically, certain chemical and radiation energy sources can cause chemical bond alterations in DNA. These alterations can and do result in production of photoproducts and chemical energy products in various parts of the genome. One such product, called an ozonide, has the catalytic properties to continuously activate cell replication, to produce mutations within the genome, and to replicate itself by autoxidation. References 1-4. This catalytic lesion in the nucleotide sequence responsible for activating the oncogene is identified herein as the primary carcinogenic lesion, and has served as the basis of the design of the compounds of the present invention. As yet, no compounds, other than those presented herein, have been designed or used specifically to dissociate the chemical bonds of an ozonide in DNA, nor are any treatment methods available that are directed toward correcting this chemical bond aberration to DNA replication, i.e., for eliminating the primary carcinogenic lesion in DNA.
There is an unmet need for a therapeutic regimen for cancer, one that is based on removing a critical lesion in one of DNA's regulatory structures and thus normalizing DNA replication and returning the regulatory system to its normal state whereby it can activate apoptosis (cell suicide). There further is an unmet need for compounds designed to be effective in such a treatment regimen. There also is an unmet need for a treatment regimen and associated compounds that are not toxic to the patient, but that instead simply eliminate the primary carcinogenic lesion and correct the regulatory aberration.